The DOI matches its Crossref record; 34 of the 34 references it cites were found in a registry or an index.
EWS/FLI-1 Silencing and Gene Profiling of Ewing Cells Reveal Downstream Oncogenic Pathways and a Crucial Role for Repression of Insulin-Like Growth Factor Binding Protein 3
Open accessAbstract
Ewing tumors are characterized by abnormal transcription factors resulting from the oncogenic fusion of EWS with members of the ETS family, most commonly FLI-1. RNA interference targeted to the junction between EWS and FLI-1 sequences was used to inactivate the EWS/FLI-1 fusion gene in Ewing cells and to explore the resulting phenotype and alteration of the gene expression profile. Loss of expression of EWS/FLI-1 resulted in the complete arrest of growth and was associated with a dramatic increase in the number of apoptotic cells. Gene profiling of Ewing cells in which the EWS/FLI-1 fusion gene had been inactivated identified downstream targets which could be grouped in two major functional clusters related to extracellular matrix structure or remodeling and regulation of signal transduction pathways. Among these targets, the insulin-like growth factor binding protein 3 gene (IGFBP-3), a major regulator of insulin-like growth factor 1 (IGF-1) proliferation and survival signaling, was strongly induced upon treating Ewing cells with EWS/FLI-1-specific small interfering RNAs. We show that EWS/FLI-1 can bind the IGFBP-3 promoter in vitro and in vivo and can repress its activity. Moreover, IGFBP-3 silencing can partially rescue the apoptotic phenotype caused by EWS/FLI-1 inactivation. Finally, IGFBP-3-induced Ewing cell apoptosis relies on both IGF-1-dependent and -independent pathways. These findings therefore identify the repression of IGFBP-3 as a key event in the development of Ewing's sarcoma.
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Gene fusion with an ETS DNA-binding domain caused by chromosome translocation in human tumours
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Self-citationLysyl oxidase: properties, specificity, and biological roles inside and outside of the cell
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Ets target genes: past, present and future
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Systematic identification of genomic markers of drug sensitivity in cancer cells
Garnett, M. J., Edelman, E. J., Heidorn, S. J., Greenman, C. D., Dastur, A., Lau, K. W., Greninger, P., Thompson, I. R., Luo, X., Soares, J., et al. (2012) · Nature · doi:10.1038/nature11005 · Cited by 2,456
Self-citationMicrosatellites as EWS/FLI response elements in Ewing's sarcoma
Gangwal, K., Sankar, S., Hollenhorst, P. C., Kinsey, M., Haroldsen, S. C., Shah, A. A., Boucher, K. M., Watkins, W. S., Jorde, L. B., Graves, B. J., et al. (2008) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0801073105 · Cited by 297
Children's Oncology Group's 2013 blueprint for research: Bone tumors
Gorlick, R., Janeway, K., Lessnick, S., Randall, R. L., Marina, N., & on behalf of the COG Bone Tumor Committee (2013) · Pediatric Blood & Cancer · doi:10.1002/pbc.24429 · Cited by 226
Guillon, N., Tirode, F., Boeva, V., Zynovyev, A., Barillot, E., & Delattre, O. (2009) · PLoS ONE · doi:10.1371/journal.pone.0004932 · Cited by 218
Self-citationNaing, A., LoRusso, P., Fu, S., Hong, D. S., Anderson, P., Benjamin, R. S., Ludwig, J., Chen, H. X., Doyle, L. A., & Kurzrock, R. (2012) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-12-0061 · Cited by 205
“EWS–FLI can bind the IGFBP3 promoter and repress its activity, further supporting the role of IGF-1R signaling in this malignancy (19).”
Metadata
- Authors
- Prieur, A., Tirode, F., Cohen, P., & Delattre, O.
- Venue
- Molecular and Cellular Biology
- Publisher
- Informa UK Limited
- Published
- 2004-08-01
- Volume
- 24
- Issue
- 16
- Pages
- 7275-7283
- ISSN
- 0270-7306 (ISSN-L)
- 1098-5549
- OpenAlex
- W2151444534
- Cited by
- 420
- References
- 34
- FWCI
- 12.75
- Type
- journal article
- Language
- en
- Open access
- green
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